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. Author manuscript; available in PMC: 2022 Jan 1.
Published in final edited form as: Behav Sleep Med. 2020 Jan 20;19(1):110–125. doi: 10.1080/15402002.2020.1714624

The Association between Insomnia and Anxiety Symptoms in a Naturalistic Anxiety Treatment Setting

Antonia N Kaczkurkin a, Jeremy Tyler b, Elizabeth Turk-Karan b, Gina Belli b, Anu Asnaani c
PMCID: PMC7369215  NIHMSID: NIHMS1551006  PMID: 31955594

Abstract

Objective/Background:

Few studies have examined the relationship between insomnia and anxiety treatment outcomes in naturalistic settings. Furthermore, prior studies typically examine insomnia within a single anxiety diagnosis without accounting for the high overlap between disorders. Here we investigate the association between insomnia and multiple anxiety disorders over a course of cognitive behavioral treatment (CBT) in a naturalistic treatment setting.

Participants:

Insomnia was assessed in 326 patients seeking treatment at a clinic specializing in CBT for anxiety.

Methods:

Multilevel modeling was used to investigate whether insomnia moderated reductions in anxiety symptoms. A cross-lagged analysis tested for bidirectional effects between insomnia and anxiety. Multiple regression was used to investigate the relationship between insomnia and anxiety while controlling for the other anxiety disorders and depression.

Results:

While there was a significant reduction in insomnia during treatment in all anxiety disorders, the majority of the most severe patients remained in the clinical range at post-treatment. Baseline insomnia did not significantly moderate anxiety outcomes, suggesting that patients with high or low levels of insomnia will do equally well in CBT for anxiety. The bidirectional effect between insomnia and anxiety did not reach significance. Additionally, posttraumatic stress disorder, generalized anxiety disorder, and panic disorder were associated with the greatest endorsement of insomnia, after controlling for the overlap between disorders.

Conclusions:

Sleep problems may persist after anxiety treatment, suggesting that CBT for insomnia may be warranted during or after a course of CBT for anxiety. Importantly, baseline insomnia does not impede anxiety reduction during CBT.

Keywords: insomnia, anxiety disorders, naturalistic samples

Introduction

Insomnia involves difficulty with initiating sleep, maintaining sleep throughout the night, or waking up early and being unable to go back to sleep which results in reduced quality or quantity of sleep (American Psychiatric Association, 2013). Insomnia is highly comorbid with anxiety (Babson & Feldner, 2010; Cox & Olatunji, 2016; Ramsawh, Stein, Belik, Jacobi, & Sareen, 2009; Roth et al., 2006; Soehner & Harvey, 2012). However, there has been a lack of research on the relationship between insomnia and anxiety during treatment (Aho, Pickett, & Hamill, 2014). Thus, the first aim of this study was to investigate the association between insomnia and anxiety over a course of cognitive behavioral treatment (CBT) for anxiety in a naturalistic treatment setting. Additionally, the research on insomnia in anxiety has often focused on a single anxiety disorder, without accounting for the high degree of overlap between anxiety disorders and depressive symptoms. Therefore, the second aim of the current study was to examine the relationship between insomnia and anxiety while controlling for the overlap between posttraumatic stress disorder (PTSD), generalized anxiety disorder (GAD), panic disorder, social anxiety disorder, obsessive-compulsive disorder (OCD), and depressive symptoms.

Theoretical models suggest a bidirectional relationship between anxiety symptoms and insomnia. A cognitive model of insomnia proposed by Harvey (2002) posits a reciprocal relationship between worrying and sleep problems. Specifically, excessive worrying about sleep and the consequences of not sleeping leads to autonomic arousal and emotional distress. This then triggers attentional processes fixated on sleep difficulties which can magnify the individual’s perception of their sleep problems. Excessive preoccupation with sleep problems coupled with counterproductive behaviors and erroneous beliefs serve to exacerbate insomnia (Harvey, 2002). The bidirectional relationship between insomnia and anxiety may differ across the anxiety related disorders of PTSD, GAD, panic disorder, social anxiety disorder, and OCD; however, some disorders have been studied more extensively than others regarding comorbid insomnia symptoms.

Research supports an association between PTSD and subjective insomnia symptoms measured with self-report (Belleville, Guay, & Marchand, 2011; Casement, Harrington, Miller, & Resick, 2012; Gehrman et al., 2013; Germain, Buysse, Shear, Fayyad, & Austin, 2004; Giosan et al., 2015; Koffel, Polusny, Arbisi, & Erbes, 2013; Krakow et al., 2001; Marcks, Weisberg, Edelen, & Keller, 2010; Roth et al., 2006). PTSD is also associated with objective measures of insomnia measured with electroencephalography (EEG), polysomnography, or actigraphy (Calhoun et al., 2007; Klein, Koren, Arnon, & Lavie, 2003; Lipinska, Timol, Kaminer, & Thomas, 2014; Mellman, Pigeon, Nowell, & Nolan, 2007; Straus, Drummond, Nappi, Jenkins, & Norman, 2015; Woodward, Murburg, & Bliwise, 2000). Specifically, sleep studies have found that individuals with PTSD are more likely to struggle with sleep maintenance and sleep efficiency as compared to healthy controls and individuals diagnosed with insomnia without PTSD (Straus et al., 2015). In terms of treatment outcomes, insomnia has been shown to persist even after successful treatment for PTSD. While insomnia symptoms improve over the course of CBT treatment for PTSD, they tend to remain within clinical levels at post-treatment (Belleville, Guay, et al., 2011; Galovski, Monson, Bruce, & Resick, 2009; Larsen, Fleming, & Resick, 2019; Pruiksma et al., 2016; Zayfert & De Viva, 2004).

Likewise, individuals diagnosed with GAD consistently demonstrate evidence of greater disturbances with their sleep when compared to healthy controls on subjective (Batterham, Glozier, & Christensen, 2012; Berger et al., 2009; Marcks et al., 2010; Ramsawh et al., 2009; Roth et al., 2006; Tempesta et al., 2013) and objective measurements (Arriaga & Paiva, 1990; Papadimitriou, Kerkhofs, Kempenaers, & Mendlewicz, 1988; Reynolds, Taska, & Sewitch, 1984). For example, individuals diagnosed with GAD are more likely to receive a comorbid diagnosis of a sleep-related disorder compared to healthy controls (Berger et al., 2009). Additionally, GAD patients are more likely to receive a diagnosis of insomnia as compared to individuals with a diagnosis of a different anxiety disorder (Marcks et al., 2010). There is also some evidence that CBT for GAD has a positive effect on insomnia symptoms (Bélanger, Morin, Langlois, & Ladouceur, 2004); however, this needs to be replicated in larger samples.

There is also support for the link between insomnia and panic disorder symptoms using subjective self-report (Batterham et al., 2012; Hoge et al., 2011; Overbeek, Van Diest, Schruers, Kruizinga, & Griez, 2005; Ramsawh et al., 2009; Roth et al., 2006; Singareddy & Uhde, 2009; Swinkels, Ulmer, Beckham, Buse, & Calhoun, 2013; Todder & Baune, 2010) and objective measures (Ferini-Strambi et al., 1996; Lauer, Krieg, Garcia-Borreguero, Özdaglar, & Holsboer, 1992; Lydiard et al., 1989; Mellman & Uhde, 1989; Sloan et al., 1999; Stein, Enns, & Kryger, 1993; Uhde et al., 1984). However, a small study of women with panic disorder found no differences in objective motor activity levels measured with an electronic wrist device during sleep compared to controls (Todder & Baune, 2010). Poor sleep quality has been associated with panic disorder in a large sample of U.S. veterans who served in Afghanistan and Iraq (Swinkels et al., 2013). In a longitudinal prospective study, insomnia was found to be significantly associated with the onset of panic disorder, suggesting that insomnia may be a risk factor for the development of panic symptoms (Batterham et al., 2012). In terms of treatment outcomes, some studies suggest that treating panic disorder does not affect comorbid insomnia symptoms (Cervena, Matousek, Prasko, Brunovsky, & Paskova, 2005).

Insomnia has been reported in individuals diagnosed with social anxiety disorder using subjective measures in both non-clinical and clinical samples (Buckner, Bernert, Cromer, Joiner, & Schmidt, 2008; Cheng et al., 2017; Raffray, Bond, & Pelissolo, 2011; Ramsawh et al., 2009; Roth et al., 2006). However, there have been very few studies that examine insomnia in social anxiety using objective measures. Of the studies using objective measures, no significant differences were found in sleep measures between individuals with social anxiety disorder and healthy controls (Brown, Black, & Uhde, 1994; Mesa, Beidel, & Bunnell, 2014); however, these studies were based on small samples. In a large sample using a national comorbidity survey, individuals with social anxiety disorder showed increased odds of reporting insomnia symptoms (Roth et al., 2006). Additionally, poorer sleep quality has predicted slower and less optimal treatment outcome for individuals receiving CBT for social anxiety (Zalta et al., 2013).

The research on insomnia in OCD using subjective measures is mixed, with some studies finding an association between OCD and insomnia (Mukhopadhyay et al., 2008; Turner et al., 2007), while others do not (Bobdey, Fineberg, Gale, Patel, & Davies, 2002). Research using objective sleep measures in OCD is also inconsistent. Some studies find abnormal sleep patterns with EEG or polysomnography (Hohagen et al., 1994; Insel et al., 1982; Kluge, Schüssler, Dresler, Yassouridis, & Steiger, 2007; Voderholzer et al., 2007); however, others report no differences between OCD and controls (Armitage et al., 1994; Robinson, Walsleben, Pollack, & Lerner, 1998). Comorbid disorders may play an important role in the relationship between OCD and insomnia. For example, in a large community sample, those with OCD showed increased odds of reporting insomnia symptoms; however, this relationship was no longer significant after controlling for comorbid mood and substance use disorders (Ramsawh et al., 2009). In terms of treatment research, to our knowledge no studies have examined the effect of Ex/RP for OCD on insomnia symptoms in adults.

A limitation of prior research on insomnia symptoms in anxiety is that many studies typically examine a single diagnostic category in isolation, without accounting for the high degree of overlap between anxiety symptom classes. There is increasing evidence that anxiety and anxiety-related disorders share many features in common (Bandelow & Michaelis, 2015; Fergus & Wu, 2010). Additionally, prior research on insomnia in anxiety disorders may be confounded with depressive symptoms, as anxiety and depression are highly comorbid (Kessler et al., 2015) and insomnia are a prominent feature of depression (Soehner & Harvey, 2012). Therefore, it would be useful to examine which anxiety disorders are associated with insomnia, while controlling for the overlap between these disorders. The benefit of this approach is that we would be able to control for the presentation of multiple diagnoses within each individual. Such an analysis would allow us to determine whether the relationship between insomnia and certain anxiety disorders is simply an artifact of comorbidity. As comorbid diagnoses are the rule rather than the exception in patients, accounting for comorbidity would be more consistent with the actual presentation of anxiety symptoms in the general population.

Together the prior research on insomnia in anxiety suggests that sleep problems are prevalent across anxiety disorders and that insomnia and anxiety may show a bidirectional relationship. However, there has been relatively less research on the association between insomnia and anxiety treatment outcomes. Therefore, the first aim of the current study was to examine the association between insomnia and anxiety during anxiety treatment in a naturalistic setting. The second aim of this study was to determine which anxiety symptom classes (PTSD, GAD, panic disorder, social anxiety disorder, or OCD) are associated with insomnia while accounting for the overlap between the anxiety disorders and depressive symptoms. Specifically, we hypothesized that 1) insomnia symptoms would decrease over the course of CBT for anxiety in all anxiety disorders; 2) insomnia would moderate treatment outcomes, with higher endorsement of insomnia being associated with less reduction in anxiety symptoms; 3) insomnia and anxiety symptom reduction would show a bidirectional effect; and 4) PTSD and GAD symptoms would be associated with the greatest endorsement of insomnia, after controlling for the other classes of anxiety symptoms and depressive symptoms.

Methods

Participants

Participants were 326 adults (age: M = 31.37, SD = 11.95) who received a diagnosis of a Diagnostic and Statistical Manual of Mental Health Disorders, Fifth Edition (DSM-5) anxiety or anxiety-related disorder at an outpatient specialty anxiety clinic in Philadelphia, PA. Frequently diagnosed disorders included posttraumatic stress disorder (PTSD), generalized anxiety disorder (GAD), panic disorder, social anxiety disorder, obsessive-compulsive disorder (OCD), specific phobia, other/unspecified anxiety disorder, and major depressive disorder. Exclusion criteria included: having a primary diagnosis other than the anxiety or related disorders listed above, having active suicidality, having a diagnosis of schizophrenia without a stable medication regimen or having more than mild current symptoms of psychosis even while on a stable antipsychotic medication regimen, evidence of intellectual disability, having diagnosis of severe autism, and evidence of active substance or alcohol dependence. Demographics of the sample are shown in Table 1. The percentages of comorbid diagnoses are presented in Table 2.

Table 1.

Sample Demographics.

N %
Gender
 Female 176 54.0%
 Male 146 44.8%
 Transgender 1 .3%
 Other 3 .9%
Race
 White 263 80.7%
 Asian 26 8.0%
 Multiracial 16 4.9%
 Hispanic 9 2.8%
 African American 8 2.5%
 Other 4 1.2%
Level of Education
 No degree 9 2.8%
 High school diploma/GED 103 31.6%
 Associates degree 12 3.7%
 Bachelor’s degree 122 37.4%
 Master’s degree 53 16.3%
 Doctoral degree 27 8.3%
Relationship status
 Single 149 45.7%
 In a relationship 53 16.3%
 Living with partner 34 10.4%
 Married 80 24.5%
 Separated 4 1.2%
 Divorced 6 1.8%
Employment status
 Full-time 130 39.9%
 Part-time 42 12.9%
 Retired 10 3.1%
 Student 93 28.5%
 Disabled 7 2.1%
 Unemployed, looking for work 16 4.9%
 Unemployed, not looking for work 20 6.1%
 Other 8 2.5%
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Table 2.

Comorbid Diagnoses

Primary Diagnosis
   Secondary Diagnosis
   Tertiary Diagnosis
N % N % N %
Obsessive-Compulsive Disorder 120 37.0% 5 2.8% 4 4.7%
Generalized Anxiety Disorder 48 14.8% 19 10.6% 9 10.5%
Social Anxiety Disorder 44 13.6% 22 12.3% 5 5.8%
Posttraumatic Stress Disorder 35 10.8% 6 3.4% 2 2.3%
Panic Disorder 25 7.7% 10 5.6% 2 2.3%
Specific Phobia 9 2.8% 7 3.9% 2 2.3%
Depressive Disorder 6 1.9% 58 32.4% 21 24.4%
Other 37 11.4% 52 29.1% 41 47.7%
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Procedures

All study procedures were approved by the Institutional Review Board at the University of Pennsylvania. Participants were screened through an initial 20 to 30-minute phone screen by a trained research assistant who assessed for anxiety symptoms and exclusion criteria (see above). Eligible patients then participated in a 2-hour intake assessment that included the Mini-International Neuropsychiatric Interview (Sheehan, Lecrubier, Sheehan, & Amorim, 1998) administered by licensed PhD/PsyD level clinicians, unlicensed PhD/PsyD clinicians (i.e., postdoctoral fellows who were working towards licensure, closely supervised by licensed clinicians), or advanced clinical psychology doctoral students in their 4th or 5th year of graduate training who were also closely supervised by licensed clinicians. In addition to this structured assessment, clinician-administered measures relevant to the patient’s presenting concern were completed (i.e., the YBOCS for OCD, PSS-I for PTSD, LSAS for social anxiety disorder) for diagnostic purposes only. Patients also completed a pre-treatment self-report questionnaire packet using a secure online database (REDCap; Harris et al., 2009) prior to their intake evaluation. Patients filled out the same self-report questionnaires at mid-treatment (roughly corresponding to week 7 after the start of treatment) and post-treatment (roughly corresponding to 19 weeks after the start of treatment, or when the patient terminated, whichever came first). Our longitudinal analyses focus on the self-report questionnaires since these were administered to all subjects at three time points, while the clinician-administered diagnostic measures were not.

Treatments

Patients were treated for their anxiety diagnosis using CBT-based treatment protocols. These evidence-based protocols primarily included treatments such as exposure and response prevention for OCD (Ex/RP; Foa, Yadin, & Lichner, 2012), prolonged exposure (PE) for PTSD (Foa, Hembree, & Rothbaum, 2007), CBT for panic (Craske et al., 2009) and social anxiety disorder (Hofmann & Otto, 2008), and mindfulness for GAD (Roemer, L. & Orsillo, 2012). Patients typically completed 10–20 sessions of individual therapy, consistent with the guidelines for treatment length in the aforementioned protocols. Non-completer status was based on the clinician’s judgement, which took several factors into account such as whether the patient stopped coming to treatment before they had reached their stated treatment goals, were non-compliant with treatment recommendations, or were resisting exposures at the top of fear hierarchies despite ongoing significant interference or distress. 27% of those who initiated therapy did not complete treatment: non-completers = 75, completers = 203, baseline only (did not start therapy) = 48. Completers and non-completers did not significantly differ in terms of age, gender, or total insomnia.

Measures

Insomnia Severity Index (ISI)

The ISI (Bastien, Vallières, & Morin, 2001) is a brief self-report measure that includes 7 items assessing the severity of sleep-onset and maintenance, insomnia, satisfaction with current sleep pattern, interference with daily functioning, noticeability of impairment, and degree of distress caused by the sleep problem. Each item is rated on a five-point Likert scale from 0 (not at all) to 4 (extremely) based on the last 2 weeks. Total scores range from 0 to 28, with high scores indicating greater insomnia severity. The ISI has shown adequate internal consistency in prior work (Cronbach’s α = .74; Bastien, Vallières, & Morin, 2001). The current sample demonstrated excellent internal consistency (Cronbach’s α ranged from .88 to .93 across the three time points).

Posttraumatic Diagnostic Scale for DSM-5 (PDS-5)

The PDS-5 (Foa et al., 2016) is a self-report measure that includes 24 items that assess PTSD symptoms and severity according to the DSM-5 criteria. Responses are rated on a 5-point Likert scale from 0 (not at all) to 4 (6 or more times a week/severe). A total score is obtained by summing the first 20 items and totals range from 0 to 80. The PDS-5 includes four subscales based on the DSM-5 symptom clusters: re-experiencing, avoidance, changes in mood and cognition, and hyperarousal. The PDS-5 demonstrates excellent internal consistency (α = .95), good test-retest reliability (r = .90), and good convergent validity with other measures of PTSD, including the PTSD Checklist, Specific Version and the PTSD Symptom Scale—Interview Version for DSM-5 (Foa et al., 2016). The PDS-5 also showed very high internal consistency in the current study (α = .94–.96).

Generalized Anxiety Disorder, 7-item scale (GAD-7)

GAD symptoms were assessed using the GAD-7 (Spitzer, Kroenke, Williams, & Löwe, 2006). The GAD-7 is a self-report measure that includes 7 items assessing the frequency of generalized anxiety symptoms rated on a scale from 0 (not at all) to 3 (nearly every day). An extra item assesses overall difficulty associated with the previously endorsed items, rated from not difficult at all to extremely difficult. The GAD-7 shows excellent internal consistency (α = .92) and good test-retest reliability in prior studies (r = .83; Spitzer et al., 2006). In the current study, the GAD-7 also showed excellent internal consistency (α = .89–.92).

Panic Disorder Severity Scale (PDSS)

Panic symptoms were assessed using the PDSS (Houck, Spiegel, Shear, & Rucci, 2002). The PDSS is a self-report measure that includes 7 items measuring dimensions of panic and related symptoms, including frequency, distress, interoceptive and agoraphobic fear and avoidance, and social/work functioning impairment. Client responses are rated on a scale of 0 (none) to 4 (extreme). The PDSS shows excellent internal consistency (α = .92) and good test-retest reliability (r = .81) in prior research (Houck et al., 2002). In the current sample, the PDSS showed excellent internal consistency (α = .92–.93).

Social Phobia Inventory (SPIN)

Social anxiety disorder symptoms were assessed using the SPIN (Connor et al., 2002), a self-report measure that includes 17 items that measure fear, avoidance, and physiological discomfort in social situations. The measure assesses discomfort in the past week on a 5-point scale ranging from 0 (not at all) to 4 (extremely). Prior research shows that the SPIN demonstrates excellent internal consistency (α = .94), good test-retest reliability (r = .90), and good convergent validity with other measures of social anxiety (Connor et al., 2002). The SPIN also showed very high internal consistency in the current study (α = .94–.95).

Obsessive Compulsive Inventory (OCI-R)

The OCI-R (Foa et al., 2002) is a self-report measure that includes 18 items assessing the presence and severity of OCD symptoms in six domains: washing, checking, ordering, obsessing, hoarding, and mental neutralizing. Items are measured on a scale from 0 (not at all) to 4 (extremely). Prior work shows that this measure demonstrates high internal consistency (α = .90) and good test-retest reliability (r = .82; Foa et al., 2002). Internal consistency for the OCI-R in the current sample was excellent (α = .89–.92).

Beck Depression Inventory II (BDI-II)

The BDI-II is a self-report measure that includes 21 items used to assess depressive symptoms (Beck, Steer, & Brown, 1996). Each item is scaled from 0 (no disturbance) to 3 (maximal disturbance). A total severity score is obtained by summing the item scores. The scale can range from minimal depressive symptoms (total scores from 0–13) to severe depressive symptoms (total scores from 29–63). In previous studies, the BDI-II shows excellent internal consistency (α = .91) and high correlations with other depression measures (Beck et al., 1996). The BDI showed very high internal consistency in the current sample (α = .93–.95).

Data Analysis

All analyses were conducted using IBM SPSS Statistics, version 25. First, we report correlations between insomnia and anxiety symptoms for each disorder: PTSD, GAD, panic disorder, social anxiety disorder, and OCD. Next, mixed-effects models were used to examine treatment outcomes. We used the linear mixed model procedures outlined in Heck, Thomas, & Tabata (2013) and Shek & Ma (2011). All measures were collected at baseline, mid-treatment, and post-treatment. We first examined whether there was a reduction in insomnia over the course of treatment. We then tested whether baseline ISI levels moderated the reduction in anxiety symptoms over the course of treatment in each anxiety disorder with sufficient a sample size (PTSD, GAD, social anxiety disorder, and OCD). Additionally, we tested for a bidirectional effect between insomnia and anxiety symptoms using cross-lagged analyses. Analyses were intent-to-treat and included all participants (completers and non-completers), as mixed-effects models are robust to missing data due to dropout. As mentioned above, 75 participants (27%) did not complete treatment in this study. Lastly, we then used a multiple regression model to determine which anxiety symptom measures (PDS-5, GAD-7, PDSS, SPIN, or OCI-R) were associated with the greatest endorsement of insomnia while accounting for the overlap between anxiety categories and controlling for depressive symptoms (BDI-II).

Prior to analyzing symptom change over time, model fitting was conducted in order to determine the best fitting shape of the growth trajectory in each measure. First, we fit unconditional growth models using linear and non-linear (quadratic, log, hyperbolic) transformations of time using maximum likelihood estimation. We compared these different transformations of time using relative Akaike’s Information Criterion (AIC) and Schwarz’s Bayesian Criterion (BIC) indices, where smaller values indicate better model fit (Heck et al., 2013). The best fitting repeated measures error-covariance structure was determined using restricted maximum likelihood estimation and comparing −2 Log Likelihood (−2LL) fit values using a chi-square test. We compared each error-covariance structure to the unstructured model. All multilevel models control for the total number of treatment sessions as each participant may have completed a different number of sessions in this naturalistic setting. Change over time was tested with the following model: Symptom measure = Number of sessions + Time. We also tested baseline ISI as a moderator of symptom reduction in four diagnostic groups with sufficient sample sizes to be tested individually (PTSD, GAD, social anxiety disorder, and OCD). Moderating effects were tested with the following model: Symptom measure = Number of sessions + Time + Time x ISI. Cross-lagged analyses were conducted to determine if insomnia levels at time t predicted anxiety levels at time t+1 or whether anxiety levels at time t predicted insomnia levels at time t+1. Lastly, we examined which anxiety symptom measure is significantly associated with insomnia, while controlling for the overlap between these measures using a single regression model: ISI = PDS-5 + GAD-7 + PDSS + SPIN + OCI-R + BDI-II.

Results

Insomnia and anxiety symptoms decreased over the course of treatment

Insomnia was highly correlated with all symptom measures including PTSD, GAD, panic disorder, social anxiety disorder, OCD, and depressive symptoms (p-values ≤ .001; Table 3). The number of patients who completed the ISI and anxiety symptom measures at each time point are shown in Table 4. ISI symptoms significantly decreased over the course of treatment across all patients (B = −1.51, SE = .27, t(431) = −5.64, p < .001). The results show a relatively linear decline in ISI scores from baseline to post-treatment. This pattern of reduction in ISI remained similar when examining each anxiety disorder individually (p-values ≤ .015) and when analyses were restricted to those with clinical levels of insomnia (ISI scores ≥ 15; B = −3.63, SE = .49, t(141) = −7.35, p < .001). 26.5% of the patients who met the threshold for clinical levels of insomnia at baseline no longer met this threshold by mid-treatment. 19.4% no longer met clinical thresholds by post-treatment, although there were fewer completed measures at the final time point.

Table 3.

Correlations between insomnia and anxiety symptom measures at baseline.

1 2 3 4 5 6 7
1. ISI ―
2. GAD-7 .45*** ―
3. PDS-5 .34*** .33*** ―
4. PDSS .38*** .51*** .40*** ―
5. OCI-R .22*** .41*** .21*** .18*** ―
6. SPIN .26*** .37*** .31*** .27*** .28*** ―
7. BDI-II .43*** .65*** .47*** .47*** .43*** .48*** ―
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Note.

*

p < .05

**

p ≤ .01

***

p ≤ .001

ISI = Insomnia Severity Index; GAD-7 = Generalized Anxiety Disorder 7-Item Scale; PDS-5 = Posttraumatic Diagnostic Scale-5; PDSS = Panic Disorder Severity Scale; OCI-R = Obsessive-Compulsive Inventory-Revised; SPIN = Social Phobia Inventory; BDI-II = Beck Depression Inventory, Second Edition.

Table 4.

Means and Standard Deviations for Each Measure at Baseline, Mid-Treatment, and Post-Treatment.

Baseline
 Mid-treatment
 Post-treatment
N M SD Range N M SD N M SD
ISI 278 10.93 6.73 0–28   169 9.24 6.51   137 7.61 6.49
GAD-7 42 12.57 5.46 0–21 27 8.67 6.55 24 7.58 5.74
PDS-5 44 47.61 16.75 0–77 41 30.34 18.56 33 14.67 14.32
OCI-R 170 23.41 12.49 0–60 100 17.36 10.78 91 10.64 9.01
SPIN 58 37.84 12.53 0–68 34 31.12 14.47 28 22.54 14.99
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Note. ISI = Insomnia Severity Index; GAD-7 = Generalized Anxiety Disorder 7-Item Scale; PDS-5 = Posttraumatic Diagnostic Scale-5; OCI-R = Obsessive-Compulsive Inventory-Revised; SPIN = Social Phobia Inventory.

Insomnia as a moderator of anxiety symptom reduction

Four disorders (PTSD, GAD, social anxiety disorder, and OCD) had sufficient sample sizes at each time point to examine insomnia as a moderator of anxiety symptom change in the relevant diagnosis-specific measure. Patients demonstrated significant reductions in their associated anxiety symptom measure (p-values ≤ .001). We then tested whether baseline ISI moderated these reductions in anxiety symptoms. Baseline ISI did not significantly moderate reductions in anxiety symptoms on any of the anxiety symptom measures: PDS-5, GAD-7, SPIN, or OCI-R (p-values ≥ .658). This suggests that those with high and low levels of insomnia show similar reductions in their anxiety symptoms.

Cross-lagged analyses to test for directional effects

Finally, we conducted cross-lagged analyses to determine whether there was a directional (or bidirectional) effect between insomnia and anxiety symptoms. While the autoregressive effects (each measure at time point t predicting the same measure at the next time point: t+1) were significant (p-values < .001), the cross-lag relationships were not significant for any of the anxiety measures (p-values ≥ .190). This suggests that insomnia levels at time t did not predict anxiety levels at time t+1 or vice versa. However, the sample size for each anxiety disorder is relatively small compared to that found in most cross-lagged analyses. Thus, our sample may be underpowered to find significant cross-lagged effects.

GAD, PTSD, and panic disorder showed significant associations with insomnia

While insomnia symptoms were common among anxiety disorders (see Table 3), a multiple regression analysis that took into account the shared variance between the anxiety disorders and that controlled for depression found that only GAD (ß = 0.24, SE = 0.07, t(319) = 3.50, p = .001), PTSD (ß = 0.13, SE = 0.02, t(319) = 2.36, p = .019), and panic disorder symptoms (ß = 0.13, SE = 0.06, t(319) = 2.18, p = .030) continued to show significant associations with insomnia after controlling for the overlap between disorders. OCD and social anxiety disorder no longer showed a significant association with insomnia after controlling for the other classes of anxiety symptoms and depressive symptoms (p-values ≥ .724). Notably, the BDI-II contains one sleep-related item, which may confound the depression results. When the sleep item is removed from the BDI-II, the results remained highly similar and continued to show that GAD, PTSD, and panic disorder were significantly associated with insomnia (p-values ≤ .023) while OCD and social anxiety disorder were not (p-values ≥ .606).

Discussion

The current study examined the association between insomnia and treatment outcomes in individuals seeking anxiety treatment in a naturalistic setting. Insomnia was significantly reduced during CBT treatment for anxiety in all anxiety and related disorders, even when restricting analyses to those with clinical levels of insomnia. However, the majority of these more severe patients continued to show clinically significant levels of insomnia at post-treatment. We also examined whether insomnia moderated the reduction of anxiety symptoms over the course of CBT treatment. Baseline insomnia did not significantly moderate anxiety symptom outcomes, suggesting that those with high levels of insomnia benefit as much from CBT treatment for their anxiety symptoms as those with lower levels of insomnia. Additionally, we used cross-lagged analyses to test for a bidirectional effect between anxiety symptoms and insomnia. The bidirectional effect between anxiety symptoms and insomnia was not significant; however, our sample may have been underpowered to examine such effects in each anxiety disorder separately. Finally, as a secondary aim, we examined which anxiety disorders were associated with the greatest endorsement of insomnia while controlling for depressive symptoms and the commonalities between anxiety disorders. We found that PTSD, GAD, and panic disorder were significantly associated with insomnia after controlling for the overlap between classes of anxiety symptoms and depressive symptoms, while OCD and social anxiety disorder no longer showed a significant association with insomnia. This suggests that the relationship between insomnia and certain anxiety disorders (OCD and social anxiety disorder) may be explained by comorbidity with other disorders with high levels of insomnia.

The results of this study are consistent with prior work suggesting that CBT for anxiety may not completely alleviate comorbid insomnia symptoms. The current study was able to show a significant reduction in insomnia symptoms over the course of CBT treatment for anxiety disorders even though therapists were not administering sleep-focused treatment, such as CBT-I. While this reduction remained significant even when restricting analyses to those with clinical levels of insomnia, the majority of the clinically severe patients remained in the clinical range of insomnia at post-treatment. This is consistent with prior studies showing that insomnia symptoms tend to remain within clinical levels after anxiety treatment, although this has been demonstrated primarily in PTSD patients (Belleville, Guay, et al., 2011; Cervena et al., 2005; Galovski et al., 2009; Larsen et al., 2019; Pruiksma et al., 2016; Zayfert & De Viva, 2004). We extend this prior work by showing similar effects in other anxiety disorders as well. The results of the current study suggest that while CBT for anxiety symptoms is associated with reductions in insomnia symptoms, anxiety treatment alone may not be sufficient to fully alleviate those symptoms. Thus, a concurrent or subsequent course of CBT-I for anxiety patients with insomnia may be warranted in those with severe levels of insomnia.

The results of the current study could be interpreted in terms of a symptom reduction hypothesis. Specifically, the relationship between insomnia and anxiety has been well-studied, and while explanations vary, insomnia is thought to be both a cause and consequence of anxiety and related disorders (Cox & Olatunji, 2016). As mentioned previously, Harvey’s cognitive model of insomnia suggests the existence of a negative feedback loop, where the detrimental effects associated with insomnia further exacerbate anxiety symptoms, subsequently leading to more insomnia (Harvey, 2002). Such a feedback loop is consistent with work showing that insomnia is associated with increased anxiety and depressive symptoms and vice versa (LeBlanc et al., 2007). Thus, reducing anxiety symptoms during CBT for anxiety disorders would then be expected to reduce insomnia. Similarly, Belleville et al. (2011) found that CBT-I administered to insomnia patients had a moderate association with reduced anxiety. Therefore, treatments that target anxiety symptoms may be expected to lead to reductions in insomnia symptoms as well.

As an alternative to the symptom reduction explanation, it is also possible that these results are due to shared mechanisms of action between CBT for anxiety symptoms and CBT-I. As noted previously, the relationship between insomnia and anxiety is thought to be bidirectional (Krystal, 2012; Seow et al., 2018), with physiological arousal and dysfunctional thoughts both contributing to this relationship (Cox, Ebesutani, & Olatunji, 2016; Harvey, 2002; Harvey & Payne, 2002). Techniques that target these underlying mechanisms and are used in both CBT and CBT-I such as relaxation, imagery, and reconceptualizing dysfunctional beliefs may be beneficial for reducing both anxiety and insomnia symptoms. Thus, the significant reduction in insomnia symptoms found during CBT for anxiety in the current study may be due to these shared treatment factors. Future work on the underlying mechanisms that both CBT and CBT-I address would be useful.

We further found that those with high levels of insomnia benefitted as much from CBT treatment for their anxiety symptoms as those with low levels of insomnia, suggesting that insomnia is not a contraindication for CBT for anxiety. This finding is counter to a previous study showing that co-occurring insomnia decreases the effectiveness of anxiety treatment (Zalta et al., 2013); however, this study was limited to social anxiety disorder patients only. Here we show evidence that baseline insomnia levels do not adversely impact anxiety reduction during CBT for anxiety across several anxiety disorders. Of note, the current study was conducted with a sample of patients with anxiety disorders and, although many patients reported insomnia symptoms, not all patients met criteria for insomnia. Therefore, these results should be replicated in a sample with more severe levels of insomnia.

Additionally, we tested the bidirectional relationship between anxiety and insomnia symptoms in each anxiety disorder. Anxiety symptoms at baseline predicted anxiety symptoms at post-treatment and, likewise, insomnia at baseline predicted insomnia at post-treatment, as expected. However, anxiety at baseline did not significantly predict insomnia at post-treatment and baseline insomnia did not predict post-treatment anxiety symptoms. Notably, each anxiety disorder was examined in a separate cross-lagged analysis, which significantly reduces the sample size. As prior work on cross-lagged analyses typically requires very large sample sizes (Hamaker, Kuiper, & Grasman, 2015), our sample may be underpowered to draw any conclusions regarding the bidirectional effect between anxiety and insomnia. Furthermore, the time points in the current study are relatively far apart; for example, the time between baseline and mid-treatment is 7 weeks. Cross-lagged analyses may be more appropriate for longitudinal studies with shorter durations between time points, such as weekly assessments.

Finally, as a secondary aim, we examined which disorders (PTSD, GAD, panic disorder, social anxiety disorder, or OCD) were significantly associated with insomnia symptoms while controlling for depression and the shared variance between anxiety disorders. When this overlapping variance is accounted for, only PTSD, GAD, and panic disorder continued to demonstrate a significant relationship with insomnia. The finding that PTSD and GAD showed significant levels of insomnia is consistent with the criteria for these disorders, which specify sleep problems. Interestingly, panic disorder also showed a significant relationship with insomnia even after controlling for overlap between disorders. While the DSM-5 does not explicitly list insomnia as a criterion for a diagnosis of panic disorder, a number of studies have reported an association between panic disorder and insomnia (Batterham et al., 2012; Hoge et al., 2011; Overbeek, Van Diest, Schruers, Kruizinga, & Griez, 2005; Ramsawh et al., 2009; Roth et al., 2006; Singareddy & Uhde, 2009; Swinkels, Ulmer, Beckham, Buse, & Calhoun, 2013; Todder & Baune, 2010). This finding may be associated with the occurrence of nocturnal panic attacks, where the symptoms of a panic attack occur at night and disrupt sleep. Between 18% and 45% of panic disorder patients report experiencing panic attacks at night without any obvious triggers (Nakamura, Sugiura, Nishida, Komada, & Inoue, 2013). In addition, the fear of bodily sensations may affect sleep in individuals with panic disorder even without a nocturnal panic attack. As this disorder is characterized by a fear of and a sensitivity to interoceptive sensations (such as heart pounding, shortness of breath, sweating, nausea, etc.), hypervigilance about these sensations may interfere with sleep. However, evidence for this hypothesis is mixed. One study found that the relationship between insomnia and panic disorder was not explained by the presence of nocturnal panic attacks (Overbeek et al., 2005), while another study showed that the combination of nocturnal panic attacks and depressive symptoms was associated with the greatest sleep problems (Singareddy & Uhde, 2009). Additional work is needed to understand the relationship between panic disorder and insomnia and the potential mechanisms driving this association.

The current study has both strengths and weaknesses. Our study was limited by the use of self-report questionnaires for symptom assessment, which could be subject to response bias. Furthermore, while our sample was diverse on other factors (e.g., gender, income level, marital status and employment status), it was not racially diverse, and thus may not be representative of some community samples in this respect. Additionally, response rates for the mid-treatment and post-treatment time points were considerably lower than at baseline. While multilevel modeling is robust to missing data, this lower response rate precluded us from conducting longitudinal analyses in panic disorder, which had insufficient data at post-treatment. Despite these limitations, our study’s strengths include the use of multilevel modeling, which is the gold standard in treatment outcome studies. An additional strength of the current study is the use of a large sample collected in a naturalistic setting, which allowed us to examine insomnia in a setting representative of outpatient clinics, where patients have multiple comorbid disorders and therapists have flexibility in the approaches they use. This “real life” setting overcomes criticisms that the rigid requirements of randomized controlled trials may compromise the external validity of treatments in the community settings they are meant to be applied (Asnaani, Benhamou, Kaczkurkin, Turk-Karan, & Foa, 2019; Hunsley & Lee, 2007; Stewart & Chambless, 2009).

Conclusions

The current study demonstrated that while insomnia decreased in all anxiety disorders during a course of CBT for anxiety, the majority of the most severe patients in the sample remained at clinically significant levels of insomnia. This study also demonstrated that those with both high and low levels of insomnia benefitted equally from CBT treatment for their anxiety symptoms, suggesting that insomnia is not a contraindication to CBT treatment for anxiety. Finally, we showed that only GAD, PTSD, and panic disorder showed significant associations with insomnia, after controlling for depressive symptoms and the shared variance between anxiety disorders. Taken together, the results of this study increase our understanding of the relationship between insomnia and anxiety in a naturalistic setting.

Acknowledgements

Dr. Kaczkurkin’s contribution is supported in part by the National Institute of Mental Health (grant number: K99MH117274), a 2017 NARSAD Young Investigator Grant from the Brain & Behavior Research Foundation, and a Penn PROMOTES Research on Sex and Gender in Health grant awarded as part of the Building Interdisciplinary Research Careers in Women’s Health (BIRCWH) grant (K12 HD085848) at the University of Pennsylvania.

The authors would like to first express their sincerest appreciation to Dr. Edna B. Foa, who is the Director and Founder of the Center for the Treatment and Study of Anxiety (CTSA) at the University of Pennsylvania, who has generously supported the integration of research into the CTSA treatment clinic and has ensured that the entire clinical team at CTSA continues to provide evidence-based treatments to patients seeking treatment at our clinic. The authors would also like to acknowledge Jody Zhong, the research assistant who assisted heavily on the original creation of the REDCap database and data infrastructure, coordinated data collection and patient reminders, and assisted with creation of the database for analysis, and Kathy Benhamou, the subsequent research assistant who enhanced this infrastructure and greatly streamlined our processes to make the data collection and database creation what it is today. We would also like to thank the current research assistant on the project, Jesse McCann, who assisted in the cleaning and set-up of the full data examined in the current study.

The authors would like to acknowledge the creators of REDCap (Harris et al., 2009), the data acquisition program used to collect the data analyzed in the present study. This software reduced burden on patients by allowing them to provide responses at home, and facilitated easier and more accurate access of treatment outcome data compared to traditional paper and pencil formats.

Finally, we would also like to deeply thank all the patients seeking treatment at our Center who were willing to allow us to analyze their deidentified data in order to better understand the efficacy of our treatments on symptom reduction and other constructs of interest throughout their treatment at our facility.

Footnotes

Declarations of interest: none

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